Georges Haddad

Georges Haddad, Ph.D.


Contact Information

Office: Numa P. G. Adams Bldg., Suite: 2309
Office Telephone: 202-806-4521
Laboratory: Numa P. G. Adams Bldg., 
Suite: 4412/4416
Laboratory Telephone: 202-806-9788


Ph.D. in Physiology (Biophysics) from University of Sherbrooke, Quebec, Canada (1993)


  • Dr. Haddad is actively involved in the teaching curriculum of the Medical, Graduate, Pharmacy, Dental and Allied Health programs in:
  • Cardiovascular Physiology
  • Cardiovascular Pathophysiology
  • Electrical Activity of the Heart
  • Arrhythmias, Heart Blocks and Myocardial Ischemia
  • Ion Channel and Intracellular Signaling


  • American Physiological Society
  • Research Society on Alcoholism
  • American Heart Association, Council on Basic Cardiovascular Sciences

Main research areas

  • Cellular and intracellular mechanisms of acute and chronic alcohol on the heart function.
  • Role of apoptotic pathways in cardiac hypertrophy and heart failure: gene therapy
  • Ionic channels and intracellular signal transduction (from the cytoplasmic membrane to the nucleus) induced by active peptides during cardiovascular hypertrophy and/or hypertension and heart failure
  • Study the pathogenic role of the renin-angiotensin system in cardiac hypertrophy and/or hypertension
  • Regulation of calcium current as well as intracellular calcium homeostasis by protein kinases and their role in cardiac hypertrophy.
  • Role of potassium channels in the metabolic response and development of the heart.

Active Grant

NIH/NIAAA grant 1 R15 AA019816-01 A1 
PI: Georges E. Haddad 
Mechanisms of alcohol-induced cardiomyopathy       
The major goal is to elucidate the role of PI3K/Akt in conveying the positive inotropic effects of low alcohol as well as the additional role of MAPK in the induction of alcoholic dysfunction with high chronic alcohol exposure. This is approached using pharmacological means and adenoviral gene targeting and therapy in vivo and in vitro. 

Research and Academic Statement

The laboratory of Dr. Haddad main focus of research is to characterize the mechanism of action of intracellular signaling pathways in alcohol-dependent-modulation of the inotropic effects of the cardiomyocytes through alterations in the activity of ion channels.   In particular, Dr. Haddad’s lab is concerned about the apoptotic and anti-apoptotic effects of beneficial effects of alcohol as well as the detrimental effects of alcohol in the development of cardiac dysfunction and heart failure. We have found that alcohol activate the MAPKs and PI3K/Akt pathways, which have been shown to play a crucial role in the progression of cardiac contractile dysfunction and failure.  Dr. Haddad’s laboratory is on the forefront of studying the interactions between these kinases to modulate ionic channels activities and survival.  On the other hand, Dr. Haddad’s laboratory have shown that not only PI3K/Akt activation is important for survival during cardiac hypertrophy and failure, but also acquires a major regulatory role on ion channels activities (IK1, IK and ICa,L).  Such effects were found to be associated with cardiac dysfunctions during cardiomyopathy.  On another note, Dr. Haddad’s Lab has undertaken an important endeavor in linking a genetic fingerprint to alcoholic cardiomyopathy in human.   One of my goals is to elucidate the intricate relationship between apoptotic pathways and their causal relationship to changes in contractility during alcoholic cardiomyopathy. This is also crucial in order to comprehend how the beneficial effects of alcohol could revert to detrimental ones in a dose- and frequency-dependent manner.  My laboratory has already fostered collaborative relationships with other investigators in the field of cardiovascular diseases, gene therapy and stem cell research which expanded our capabilities.

On the Educational front, Dr. Haddad has served as the Director of Graduate Studies and mentoring undergraduate, graduate and professional students in research related to cardiac hypertrophy.  Dr. Haddad has founded the Cardiovascular Summer Research Program at Howard University through which he mentored meritorious students from all over the USA.  Dr. Haddad also chaperoned few students to attend scientific meetings, such as the Experimental Biology, for exposure and training purposes.  Dr. Haddad is involved in the Honors and the Amgen programs at Howard University, mentoring and guiding students on cardiac hypertrophy and heart failure research throughout the academic year and even in the summer.  

Selected peer-reviewed publications

  1. Nsini A. Umoh., Robin K., Richard M. Millis, Mustafa Al-Rubaiee M., Pandu Gangula, and Georges E. Haddad (2014).  Cacitonin gene-regulated peptide regulates cardiomyocyte survival through regulation of oxidative stress by PI3K/Akt and MAPK signaling pathways.  Annals of Clinical and Experimetal Hypertension (in Press).
  2. Vernon Bond Jr., Bryan H. Curry, Richard G. Adams, Richard M. Millis and Georges E. Haddad (2014). Cardiorespiratory function associated with dietary nitrate supplementation. Applied Physiology, Nutrition, and Metabolism 39(2): 168-172.
  3. Robin K. Walker, Valeire M. Cousins, Nsini A. Umoh, Miara A. Jeffress, Delaram Taghipour, Mustafa Al-Rubaiee, Georges E. Haddad (2013). The good, the bad and the ugly with alcohol use and abuse on the heart.  ACER J. 37 (8)1253-1260.
  4. Bond V Jr, Curry BH, Adams RG, Asadi MS, Millis RM, Haddad GE (2013).  Effects of dietary nitrates on systemic and cerebrovascular hemodynamics. Cardiol. Res. Pract. 2013:435629.
  5. Mustafa Al-Rubaiee, Pandu R. Gangula, Richard M. Millis, Georges E. Haddad (2013).  Inotropic and Lusitropic effects of Calcitonin Gene-Related Peptide in the heart.  AJP-Heart and Circ. Physiol. 304: H1525-H1537.
  6. Gangula PR, Dong YL, Al-Hendy A, Richard-Davis G, Montgomery-Rice V, Haddad G, Millis R, Nicholas SB, Moseberry D (2013).   Protective cardiovascular and renal actions of vitamin D and estrogen.  Frontiers in Biosciences (Schol Ed.) 5:134-148.
  7. Richard Millis, Alvin Zikiar, Aiqiu Zhao and Georges E. Haddad (2012). Effects of IGF-1 on IK and IK1 Channels via PI3K/Akt Signaling in Neonatal Cardiac Myocytes.  Int. J. Cell. Biol., Vol. 2012, 712153.